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Nutritional implications of dietary interactions: A review

Benjamin Caballero


A large number of dietary interactions have been described. Of these, only a relatively small number have been proved of relevance for human nutrition under the conditions of real diets. These interactions most often occur at the intestinal lumen, but they may also take place during utilization or storage of nutrients. Traditional diets of developing countries, which usually include non-refined cereals and other sources of fibre, may inhibit the bioavailability of mineral nutrients, contributing to specific deficiencies. Drug-nutrient interactions may also impact on nutritional status, particularly in population groups such as the elderly, who frequently receive prolonged medication and may have an inadequate food intake.



Foods constitute a complex chemical and biological mix resulting from the interaction of natural constituents, industrial processing, and household preparation. All of these cause marked changes in the physico-chemical properties of a meal, and thus determine the amount and the bioavailability of nutrients. Further, diet constituents continue to interact in the gastrointestinal tract and at the level of intermediary metabolism. Since many recommendations for nutrient intake are based on studies using isolated nutrients or purified test meals, they do not necessarily reflect the requirements in terms of actual meals consumed by individuals. The study of dietary interactions is of particular importance for developing countries, where food preparation and dietary habits vary widely, and where there is a need to optimize the nutrient utilization.

Virtually any nutrient can cause adverse effects if ingested in excessive amounts. Such undesirable effects may depend on the inherent toxicity of the excess intake, but often they are caused by the antagonistic effect of the excess nutrient on the bioavailability of other dietary components. Likewise, non-nutritional substances, such as drugs or natural contaminants, can interfere with nutrient utilization. This area has received extensive attention in the past decades, particularly in relation to animal nutrition. These studies, although not always relevant to human nutrition, have stimulated clinical investigators to explore dietary interactions in the context of human nutritional physiology.


Nutrient-nutrient interactions

Although the term interaction denotes a bidirectional effect, many interactions are unidirectional, i.e., one nutrient affects the biological disposition of another, which remains more or less passive. Bidirectional interactions are most common among nutrients with similar physico-chemical properties and sharing a common mechanism of absorption or metabolism; finally, some uni- or bidirectional interactions are affected by the presence of a third dietary constituent. Nutrient interactions are not usually additive. For example, both haem iron and ascorbic acid taken separately increase the absorption of non-haem iron; however, simultaneous ingestion of both does not increase non-haem iron absorption more than each one does alone [1]. A selected summary of nutrient-nutrient interactions is presented in table 1.

TABLE 1. Dietary interactions affecting nutrient bioavailability

Reported effects
Vitamin A
protein Protein deficiency decreases intestinal
absorption of vitamin A. [15]
Diets with low (< 10%) or high
(20% -40% ) protein content inhibit
carotene dioxigenase activity.
Optimum activity was found at a
P% of 10. [16]
Protein deficiency decreases the
capacity to release retinol from
river stores. [17]
Lysine-deficient proteins decrease
plasma retinol levels. [18]
Protein quality affects the rhythm of
depletion of liver vitamin A reserves.
Corn- and black bean-based diets
cause lower rate of depletion than
casein, even when they provide more
protein. [19]
fat An increase in dietary fat content
increases carotene absorption. [20]
Polyunsaturated fats inhibit carotene
absorption and metabolism. [21]
vitamin E Supplementation with vitamin E at
moderate doses protects against
the teratogenic and toxic actions of
vitamin A. [22, 23]
Supplementation with vitamin E in
creases liver storage of vitamin A.
Vitamin E supplementation improves
plasma vitamin A levels in children
with vitamin A deficiency. [25]
Vitamin E deficiency accelerates the
depletion of liver vitamin A stores.
Supplementation with 200 IU vitamin E
per day during 3 weeks decreases
serum vitamin A levels. [27]
147 mg vitamin E for 3 weeks decreases
serum retinol levels. [28]
zinc Zn supplementation improves scores in
the dark adaptation test. [29]
Vitamin B6
protein The level of protein intake is inversely
correlated with plasma B6 and piridoxal
phosphate levels, and with the
urinary excretion of 4-pindoxic acid.
Diets providing the same amino acid
pattern as corn cause a decrease of B6
concentration in plasma and of PLP
in liver. [31]
dietary fibre Ingestion of 15 g fibre per day during 18
days causes a fall in plasma levels of
B6 and PLP, as well as a rise in faecal
excretion of the vitamin. [32]
Vitamin E
vitamin C Vitamin C acts synergistically in the
intracellular antioxidant system to
regenerate reduced tocopherol. [33]
protein Addition of protein to the diet (fish,
poultry, meat) increases the absorp
tion of non-haem iron. [34]
amino acids Different amino acid mixtures promote
iron absorption. Cysteine is one of
the most efficient. [35, 36]
organic acids Diets with relatively low pH or with
elevated lactic acid content enhance
iron absorption. [37, 38]
phosphate Calcium phosphate decreases iron
absorption, but inorganic P has no
effect. [39]
zinc Use of Zn supplements inhibits iron
absorption. [40]
Iron absorption form a Zn-Fe supple
ment decreases progressively as the
Zn:Fe ratio increases. [41]
vitamin C Favours the absorption of non-haem
iron by binding and solubilizing it at
the physiological intestinal pH. [42]
Facilitates iron mobilization by inhibit
ing ferritin breakdown at the lysosome. Vitamin C deficiency causes
iron accumulation as haemosidenn.
[43, 44]
vitamin A Vitamin A deficiency inhibits iron
utilization and accelerates the
development of anaemia. [45]
Iron deficiency is epidemiologically
associated with vitamin A deficiency.
Rats deficient in vitamin A exhibit iron
accumulation in liver and spleen. [47]
Vitamin A fortification improves the
haematological indices of popula
tions. [48]
tea, coffee Simultaneous administration of tea
decreased iron absorption from
bread from 10.4% to 3.3%. This
effect is due to the formation of iron
tanates in the intestinal lumen. [49]
tea, coffee One cup of coffee significantly de
creases the absorption of one dose of
iron. This effect is proportional to the
coffee concentration in the solution.
polyphenols They bind and insolubilize iron. Vegetables
with high polyphenol content
may have low iron bioavailability.
[51, 52]
protein Favours Zn absorption by decreasing
the inhibitory action of phytates. [53]
Malnourished children treated with
soy-based protein diets exhibit lower
plasma Zn levels and slower rate of
weight gain. [54]
A soy-based test meal decreases the
absorption of 65-Zn in healthy sub
jects. [55]
On the other hand, studies using texturized
soy protein meals extrinsically labelled with
65-Zn showed the same Zn absorption as
animal protein diets. [53]
The bioavailability of 70-Zn from liquid
soy-based diets was similar to control diets.
amino acids Several amino acids increase Zn
absorption, possibly by facilitating
the mineral's release from the
Ca-phytate-Zn complex. [57]
Histidine is one amino acid that inhibits
Zn absorption, by forming insoluble
complexes. This action may be
antagonized by adding other amino
acids or protein to the diet. [58]
folate A 40 miug/day folate supplementation in
creases faecal Zn losses in men. [59]
A 350 miug/day folate intake during 2
weeks decreases Zn absorption in
healthy adults. [60]
Zinc absorption was decreased in a
group of pregnant women receiving
standard iron-folate supplements.
iron Non-haem iron administration decreas
es inorganic zinc absorption. [61]
A Fe:Zn ratio of 2:1 or higher
lowers the plasma response curve
to a 25 mg oral Zn dose. The iron
compound with the most potent
inhibitory action on Zn absorption
was ferrous sulphate. [62]
iron The iron salt NaFeEDTA decreases the
plasma response curve after ingestion
of 25 mg Zn. [63]
Haem iron has no inhibitory effect on
Zn absorption. [64]
Supplementation of healthy infants
with 30 mg iron per day during 3
months had no effect on serum zinc
levels. [65]
Mineral supplements commercially
available may have Fe:Zn ratios
of up to 30:1, making their Zn availability
negligible. [66]
tin 50 mg oral stannous sulphate decreases
Zn absorption (by balance) in normal
subjects. [67]
Other studies, however, found that
Sn:Zn ratios of up to 8:1 had no
effect on the plasma response curve
to a 12.5 mg oral dose of Zn sulphate.
calcium Animal studies found an inhibition of
intestinal Zn absorption by dietary
Ca. [68]
Increases in dietary Ca intake from
3 to 6 g per kg per day had a significant
effect on Zn bioavailability, possibly due to
the formation of Ca-Zn-phytate complexes.
[69, 57]
Calcium prolongs the effects of phytates
by slowing their intestinal breakdown
by phytases. [70, 71]
Studies in normal subjects receiving up
to 2 g Ca per day showed no effect on
Zn absorption. [72]
As an indirect indication of the an
tagonist action of Ca on Zn bioavailability, it
has been shown that cow's milk decreases Zn
absorption. [73]


Zinc deficiency has been described in
populations ingesting adequate
amounts of the mineral but very high
levels of dietary fibre and phytates.
The inhibitory action of phytates on
Zn absorption is also related to the
calcium content of the diet. [74]
A Ca-phytate-Zn ratio of 0.4-0.6 can
decrease Zn absorption, and ratios
over 3.0 may cause Zn deficiency.
magnesium Antagonizes Zn absorption by a
mechanism similar to that of Ca. [76]
wine At moderate doses, table wine en
hances Zn absorption. This effect is
independent of its alcohol content,
since dealcoholized wine has the
same effect as regular wine. [77]
protein Dietary protein stimulates urinary Ca
excretion. [78]
A moderate increase in dietary protein
intake, from 65 to 94 g per day during
28 days does not affect calcium balance in
healthy subjects. [79]
fat Decreases Ca absorption by forming
insoluble soaps. Inhibitory action is
much less with triglycerides than with
free fatty acids. [80]


Cellulose administration increases
faecal Ca excretion. [81]
Use of partially refined flour lowers Ca
absorption. [82]
Dietary fibre is a more potent inhibitor
of Ca absorption than phytates. [83, 84]
lactose Stimulates calcium absorption in many
animal models. Less clear effects
found in human studies. [85-87]
zinc Zinc supplements of 140 mg per day
lower Ca absorption significantly
when Ca intake is low (230 mg per
day), but have no effect at Ca intake
of 800 mg per day. [48]
sodium Increases in NaCI intake increase urin
ary Ca excretion and lower serum Ca
in subjects with hypercalciuria. [88]
Low-sodium diets reduce urinary
Ca excretion in hypercalciuric
individuals. [89]
An increase in salt intake in normal
subjects increases urinary Ca excretion. [90]
protein Fractional absorption of a 3 mg dose
of Cu is 36% when the diet provides
50 g protein, and 52% when protein intake is increased to 150 g.
Cu retention increases similarly
in response to dietary protein. [91]
Minimum Cu requirement for balance
decreases from 1.5 to 1.33 mg per
day when dietary protein is in
creased from 40 to 100 g per day.


Subjects consuming a low-Cu diet
(1 mg per day) had significantly lower
erythrocyte superoxide dismutase
activity when the diet provided 20%
fructose than when it provided 20%
starch. [92]
vitamin C Supplementation with 1.5 g ascorbic
acid per day for 64 days causes a significant
fall in ceruloplasmin levels,
and has a similar but less marked
effect on serum Cu levels. [2]
zinc Cu requirements for balance in healthy
subjects increase from 0.89 to 1.64
when Zn intake is increased from 5
to 20 mg per day. [93]
Chronic Zn supplementation can cause
Cu deficiency. [94, 40]
Increases in dietary zinc intake up to
10-15 mg per kg per day decrease
copper absorption in adolescent
females. [95]
However, roughly similar levels of Zn
intake did not affect Cu balance in
healthy adult women. [96]
dietary fibre Addition of 14 g of hemicellulose to the
diet of healthy adolescents signif
icantly increases faecal Cu losses.
calcium Magnesium utilization is decreased
when calcium intake increases. [98]

From the physiological standpoint, nutrient interactions can occur at several different levels:

For example, it has been reported that 1.5 g of vitamin C for 64 days significantly lowers ceruloplasmin levels and also decreases serum copper concentration [2].

Interactions with dietary fibre

Dietary fibre has been a focus of interest in the past decade, primarily because of epidemiological data suggesting a protective effect against chronic diseases of the gastrointestinal tract. Such effect appears to be related to dietary fibre but not phytate content, though these two components are frequently present together in most fibre-rich foods.

Fibre has a significant inhibitory effect on the absorption of minerals, and it also lowers the plasma glucose response curve after sucrose intake. Some of its actions on nutrient absorption can, therefore, be beneficial in the dietary management of diseases such as diabetes and hypercholesterolaemia. The role of fibre in the bioavailability of selected nutrients is included in table 1.

Dietary fibre can also indirectly affect nutrient absorption by modulating gastrointestinal physiological functions such as motility, acid secretion, and hormone release. Actions reported for different types of fibres are described in table 2.

TABLE 2. Effects of dietary fibre on gastrointestinal function

Function Effects
Fibre increases the rate of gastric
filling. [99,100]
Insoluble fibre increases transit time.
Viscous fibre decreases transit time in rats.
Addition of pectin to the diet
decreases serum levels of GIP
and enteroglucagon in response to
a 60 g oral glucose load. [103]
Administration of insoluble fibre
decreases serum levels of GIP and
glucagon. Viscous fibre has a similar effect on
GIP but does not affect glucagon levels.
Addition of fibre to the diet increases
gastrin secretion. [106]
Fibre decreases the activity of
pancreatic enzymes, possibly by
modifying pH optimum and
enzyme-substrate interaction.
[107, 108]
Decreases the activity of alkaline
phosphatase in the microvilli. [109]
Decreases disaccharidase activity.
Decreases lactase activity. [111]
Decreases surface hydrolysis in the
intestinal mucosa. [112]
Increases resistance to the passage of
substances through the unstirred
water layer. [113]
Stimulates the production of intestinal
mucin. [108]
Viscous fibre binds bile acids, but in
soluble fibre has much less binding
activity. [114,115]
Decreases the rate of absorption of
carbohydrates, thus lowering the
amplitude of the plasma glucose
response curve. However, total
carbohydrate absorption in a
period of 8 hours postingestion is
not effected. [116,117]
Metabolism Long-term consumption decreases
plasma glucose levels and insulin
requirements in diabetics. [104]
Supplementation with insoluble
fibre for 30 days improves glucose
tolerance. [118]
Inhibits intestinal cholesterol and
phospholipid synthesis. [119]

The natural fibre content of foods may be significantly affected by processing. For example, an extraction rate of 70% in the refining of wheat flour may remove over 60% of its fibre and phytate content [3]. Different processing methods may affect certain interactions to different degrees. For instance, zinc bioavailability from soy protein sources is significantly higher from acid-precipitated than from neutralized concentrates [4, 5].

Implications for developing countries

While in developed societies the issue of nutrient interactions usually pertains to special situations, such as total parenteral nutrition or chronic malabsorptive disease, in developing countries diet interactions may play an important role in determining the nutritional status of large population groups. Thus, the problem of low nutrient intake in these societies is compounded by the presence of inhibitory factors in the diet. The classic description of zinc deficiency in rural populations of Iran consuming very high amounts of dietary fibre is an example of this [6], as is iron deficiency in many Latin American populations, in which a marginal nutrient intake becomes grossly inadequate due to inhibited bioavailability.

These factors have important practical implications for defining dietary guidelines in developing countries. For example, while guidelines for developed societies recommend increasing the intake of dietary fibre, this item constitutes a negative factor in the traditional diets of developing countries because it inhibits the absorption of iron and other minerals. Furthermore, food processing that reduces the fibre content of cereals (e.g. high-extraction flours) usually removes a significant proportion of essential nutrients such as calcium, magnesium, and folates [3]. Urbanization and population migration will also have a strong impact on dietary practices, eliminating some adverse dietary interactions and creating new ones.


Drug-nutrient interactions

Drug-nutrient interactions arise primarily from the continuous use of prescription medications, but also from drugs added regularly to the food chain. Some of these are naturally present in foods, but the majority are introduced, deliberately or as contaminants, during industrial processing. For example, pesticide residues can be found not only in agricultural products but also in human milk [7]. Drugs such as hormones and antibiotics are routinely used to protect and improve cattle and poultry production. In some cases, metabolites of these compounds persist and can be found in the human diet, as is the case with estrogen residues, which have been suggested as potentially carcinogenic [8]. Antibiotic contaminants can eventually favour the development of resistant strains and increase the risk of infections, particularly in persons with deficient immune response. These forms of contamination are usually more serious in developing countries, due to inadequate controls or regulations. It should also be noted that the interaction between non-nutritional and nutritional dietary substances is operative both ways: a deficient nutritional status greatly enhances the toxicity of contaminants such as pesticides [9]. Very little is known about the long-term consequences of these complex interactions at the population level.

Many prescription drugs can have an impact on nutritional status by interfering with the absorption or utilization of specific nutrients. Such potential adverse effects are not always considered by the healthcare providers who prescribe medications. Likewise, those responsible for the nutritional management of patients may not associate changes in their nutritional status with the adverse consequences of medications, or these effects may be masked by the symptoms of the underlying disease process. Table 3 summarizes the nutritional effects of several commonly used drugs.

TABLE 3. Nutritional effects of some commonly used drugs

Drug Nutrient affected Effects
vitamin D
Decrease serum vitamin D levels by activating the P-450
oxidative system in liver. May cause osteomalacia and
Folic acid Decrease absorption and serum levels of folates by inhibiting
vitamin B12 intestinal conjugase activity. Inhibit B12 transport. May cause neuropathy and megaloblastic anaemia.
Copper Increase its serum levels.
Barbiturates calcium Increase vitamin D requirements by increasing its
vitamin D Degradation. Increase bone resorption and may cause osteomalacia.
Thiamine Decrease its intestinal absorption.
Vitamin C Increase its urinary losses.
Cobalamine Decrease serum levels. Prolonged use may lead to megaloblastic anaemia.
Corticosteroids calcium Inhibit intestinal absorption and increase urinary excretion
phosphorus of calcium and phosphorus. High doses and chronic use
vitamin D may decrease serum 1,25-(OH)2-D3 levels and cause osteoporosis.
nitrogen May lead to negative nitrogen balance by increasing urinary nitrogen losses.
minerals Increase urinary zinc excretion and decrease its serum level.
Increase their serum levels.
glucose Increase its plasma levels. Impair glucose tolerance.
Oral contraceptives vitamin C Decrease ascorbic acid concentration in plasma, platelets, and leukocytes.
folic acid
vitamin B12
Decrease their serum levels. May cause megaloblastic anaemia.
amino acids Impair tryptophan metabolism. May change plasma amino acid profile.
vitamin A
vitamin E
Increase their serum levels.
copper Increase its serum levels.
Salycilates vitamin C Decrease its concentration in serum and platelets.
vitamin K Antagonize its action on the coagulation system.
amino acids Decrease their intestinal absorption, particularly that of

tryptophan; increase their urinary excretion.

oxacillin, etc.)
potassium At high doses may cause hypokalaemia by increasing urinary potassium losses.
fats Oxacillin may cause steatorrhoea.
Tetracycline minerals Inhibit intestinal absorption of iron, calcium, zinc, and magnesium. Act as chelating agents and also inhibit synthesis of transport proteins at the enterocyte.
Fats Decrease their intestinal absorption.
vitamin K Decrease its availability from intestinal bacteria.
vitamin C Increase urinary losses and decrease its concentration in plasma and leukocytes.
Chloramphenicol iron Increases its serum level, as well as total iron binding capacity.
folic acid Antagonizes their physiological action, increasing requirements.
vitamin B12 Increases its requirements. May cause peripheral neuropathy.
kanamicin fats
vitamins A, D, K
vitamin B12
Causes malabsorption of these nutrients.
gentamicin magnesium Increases urinary losses of these electrolytes and may lead to
potassium Hypomagnesaemia and hypokalaemia.
neomycin fats Causes malabsorption of these nutrients. Decreases plasma
vitamins A, D, K
vitamin B12
B12 levels. Acts by precipitating bile salts and interfering with mycellar formation.
Decreases their intestinal absorption.
paromomycin fats Decreases their absorption and hepatic transport.
sulfas folic acid Decrease its intestinal synthesis, absorption, and serum levels. Impair the response to folate supplementation, and thus increase the requirements of this nutrient.
Atropin iron Inhibits its intestinal absorption.
Indomethacin vitamin C

amino acids

Decreases its plasma levels in plasma and platelets. Decreases their intestinal absorption.
Al hydroxide

Ca carbonate

Na bicarbonate

Mg trisilicate

thiamine Affect its bioavailability, since thiamine is unstable at high pH.
iron Decrease its intestinal absorption.
phosphorus Aluminium-containing antacids inhibit phosphate absorption and may cause P depletion.
vitamin A Aluminium-based antacids inhibit its intestinal absorption.
fats Calcium carbonate may cause steatorrhoea.

Therapeutic agents may modify nutrient status at several levels:

Some drug-nutrient interactions occur only when nutrient and drug are ingested concurrently, as is the case with drugs affecting nutrient availability by changing the intestinal pH. In other cases, a relatively long period of exposure is required to observe an effect, as for example corticosteroid action on skeletal calcium. The interactions between drugs and nutrient absorption and metabolism have been recently reviewed by Roe [10].

Drug-nutrient interactions in the opposite direction, i.e. nutrients affecting drug action, are also possible. Protein and carbohydrate intake alters the rate of excretion, and consequently the half-life of several drugs [11] Dietary amino acids may inhibit the entry of drugs into the brain by competing for transport at the blood-brain barrier [12]. Dietary fat affects the free fraction of drugs by competing for albumin binding, which may modify their uptake by target tissues [13]. Some foods (notably certain cheeses) may contain natural biogenic amines that can cause sympathetic symptoms when consumed by persons receiving monoamine oxidase inhibitors [14].

Any condition in which drug clearance is impaired, such as liver or kidney disease, enhances the possibility of a drug-nutrient interaction if drug levels are not adequately monitored. The effects of therapeutic drugs in patients with severe protein-energy malnutrition or diarrhoea have not been extensively studied, but since protein-energy malnutrition causes alternations in several detoxifying processes, it must be assumed that such patients are at greater risk of developing adverse drug-nutrient interactions at lower drug doses than healthy individuals.

A group that is especially vulnerable to the adverse nutritional effects of drugs is the elderly. This is because they frequently receive chronic medications, usually with more than one drug. Furthermore, their dietary intake may frequently be only marginally adequate because of anorexia, little physical activity, medical problems, or socio-cultural difficulties.



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